The Role of Mac-2 Binding Protein in Oral Cancer Migration

碩士 === 長庚大學 === 生物醫學研究所 === 100 === Mac-2 binding protein (Mac-2 BP) is a secreted glycoprotein of 90-100 kDa. Although elevated Mac-2 BP levels have been observed in tissues and sera of patients with various cancer types, the functions of Mac-2 BP remain largely unknown. Previous study from our lab...

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Main Authors: Chih Yen Kan, 闞之言
Other Authors: J. S. Yu
Format: Others
Published: 2012
Online Access:http://ndltd.ncl.edu.tw/handle/70773811677590625671
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spelling ndltd-TW-100CGU051140982017-01-22T04:14:29Z http://ndltd.ncl.edu.tw/handle/70773811677590625671 The Role of Mac-2 Binding Protein in Oral Cancer Migration 探討Mac-2 binding protein在口腔癌移動中扮演之角色 Chih Yen Kan 闞之言 碩士 長庚大學 生物醫學研究所 100 Mac-2 binding protein (Mac-2 BP) is a secreted glycoprotein of 90-100 kDa. Although elevated Mac-2 BP levels have been observed in tissues and sera of patients with various cancer types, the functions of Mac-2 BP remain largely unknown. Previous study from our lab revealed that Mac-2 BP is overexpressed in oral squamous cell carcinoma (OSCC) and could be highly secreted by OSCC cell lines. Furthermore, Mac-2 BP knockdown in OEC-M1 caused drastic inhibition of cell migration, suggesting that Mac-2 BP may play an important role in the mobility of OSCC cells. In this study, we investigate the global effect of Mac-2 BP knockdown in OC3 cells on the total cell proteome and the secreted proteome (secretome). Since previously researches have reported that ECM-integrin signaling pathway may improve cell mobility, these data imply that Mac-2 BP may participate in ECM-integrin signaling pathway, and stably knocked down Mac-2 BP alters cell mobility by regulating cell adhesion or blocking the signal transduction. Quantifying confocal microscope image of immunofluorescence staining indicated that the average size but not the number of focal adhesions was larger in Mac-2 BP knockdown (KD) cells than in control cells. However, we could not observe the difference in cell adhesion function. Moreover, FAK activation of Mac-2 BP knock down cells showed low sensitivity to FN stimulation, although the phenomenon is not significant. These results demonstrate that Mac-2 BP may affect multiple pathways, and the slightly change of adhesive ability is not the main factor for altering cell mobility. Additionally, the bioinformatics analysis show the dramatic change of secretome in Mac-2 BP KD cells, which may be caused by exceptional transportation and secretion. These results indicate that Mac-2 BP may in turn affect cell mobility by varying the signal equilibrium. J. S. Yu 余兆松 2012 學位論文 ; thesis 109
collection NDLTD
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sources NDLTD
description 碩士 === 長庚大學 === 生物醫學研究所 === 100 === Mac-2 binding protein (Mac-2 BP) is a secreted glycoprotein of 90-100 kDa. Although elevated Mac-2 BP levels have been observed in tissues and sera of patients with various cancer types, the functions of Mac-2 BP remain largely unknown. Previous study from our lab revealed that Mac-2 BP is overexpressed in oral squamous cell carcinoma (OSCC) and could be highly secreted by OSCC cell lines. Furthermore, Mac-2 BP knockdown in OEC-M1 caused drastic inhibition of cell migration, suggesting that Mac-2 BP may play an important role in the mobility of OSCC cells. In this study, we investigate the global effect of Mac-2 BP knockdown in OC3 cells on the total cell proteome and the secreted proteome (secretome). Since previously researches have reported that ECM-integrin signaling pathway may improve cell mobility, these data imply that Mac-2 BP may participate in ECM-integrin signaling pathway, and stably knocked down Mac-2 BP alters cell mobility by regulating cell adhesion or blocking the signal transduction. Quantifying confocal microscope image of immunofluorescence staining indicated that the average size but not the number of focal adhesions was larger in Mac-2 BP knockdown (KD) cells than in control cells. However, we could not observe the difference in cell adhesion function. Moreover, FAK activation of Mac-2 BP knock down cells showed low sensitivity to FN stimulation, although the phenomenon is not significant. These results demonstrate that Mac-2 BP may affect multiple pathways, and the slightly change of adhesive ability is not the main factor for altering cell mobility. Additionally, the bioinformatics analysis show the dramatic change of secretome in Mac-2 BP KD cells, which may be caused by exceptional transportation and secretion. These results indicate that Mac-2 BP may in turn affect cell mobility by varying the signal equilibrium.
author2 J. S. Yu
author_facet J. S. Yu
Chih Yen Kan
闞之言
author Chih Yen Kan
闞之言
spellingShingle Chih Yen Kan
闞之言
The Role of Mac-2 Binding Protein in Oral Cancer Migration
author_sort Chih Yen Kan
title The Role of Mac-2 Binding Protein in Oral Cancer Migration
title_short The Role of Mac-2 Binding Protein in Oral Cancer Migration
title_full The Role of Mac-2 Binding Protein in Oral Cancer Migration
title_fullStr The Role of Mac-2 Binding Protein in Oral Cancer Migration
title_full_unstemmed The Role of Mac-2 Binding Protein in Oral Cancer Migration
title_sort role of mac-2 binding protein in oral cancer migration
publishDate 2012
url http://ndltd.ncl.edu.tw/handle/70773811677590625671
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